Lipid Metabolism Modulation during SARS-CoV-2 Infection: A Spotlight on Extracellular Vesicles and Therapeutic Prospects

D’Avila, Heloisa; Lima, Claudia Natércia Rocha; Rampinelli, Pollianne Garbero; Mateus, Laiza Camila Oliveira; Sousa Silva, Renata Vieira de; Correa, José Raimundo; Almeida, Patrícia Elaine de

doi:10.3390/ijms25010640

Cited by 8 publications

(5 citation statements)

References 159 publications

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“…Taken together, viral infection may reduce adipocyte size in SAT and VAT, and vaccination has no effect on the adipocyte size area. Studies on COVID-19 patients have shown dysregulated lipid profiles, which are associated with an increased risk of severe consequences [ 10 , 20 , 21 , 22 ]. It has been suggested that modulation of cellular lipid metabolism could be a therapeutic target for SARS-CoV-2 infection [ 20 , 22 ].…”

Section: Discussionmentioning

confidence: 99%

“…Studies on COVID-19 patients have shown dysregulated lipid profiles, which are associated with an increased risk of severe consequences [ 10 , 20 , 21 , 22 ]. It has been suggested that modulation of cellular lipid metabolism could be a therapeutic target for SARS-CoV-2 infection [ 20 , 22 ]. However, the influence of the infection on lipid metabolism, lipolysis, and lipogenesis in adipocytes remains unclear.…”

Section: Discussionmentioning

confidence: 99%

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Consequences of COVID-19 on Adipose Tissue Signatures

Krupka,

Hoffmann,

Jasaszwili

et al. 2024

IJMS

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Since the emergence of coronavirus disease-19 (COVID-19) in 2019, it has been crucial to investigate the causes of severe cases, particularly the higher rates of hospitalization and mortality in individuals with obesity. Previous findings suggest that adipocytes may play a role in adverse COVID-19 outcomes in people with obesity. The impact of COVID-19 vaccination and infection on adipose tissue (AT) is currently unclear. We therefore analyzed 27 paired biopsies of visceral and subcutaneous AT from donors of the Leipzig Obesity BioBank that have been categorized into three groups (1: no infection/no vaccination; 2: no infection but vaccinated; 3: infected and vaccinated) based on COVID-19 antibodies to spike (indicating vaccination) and/or nucleocapsid proteins. We provide additional insights into the impact of COVID-19 on AT biology through a comprehensive histological transcriptome and serum proteome analysis. This study demonstrates that COVID-19 infection is associated with smaller average adipocyte size. The impact of infection on gene expression was significantly more pronounced in subcutaneous than in visceral AT and mainly due to immune system-related processes. Serum proteome analysis revealed the effects of the infection on circulating adiponectin, interleukin 6 (IL-6), and carbonic anhydrase 5A (CA5A), which are all related to obesity and blood glucose abnormalities.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Consequences of COVID-19 on Adipose Tissue Signatures

Krupka,

Hoffmann,

Jasaszwili

et al. 2024

IJMS

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“…These findings may represent the cellular changes induced by the virus to facilitate its replication, as demonstrated in recent in vitro studies [ 68 , 69 ]. The virus may exploit endogenous lipid components in various forms (i.e., lipoproteins and exosomes) as “Trojan horses” to facilitate immune evasion in their systemic dissemination [ 70 , 71 ]. In contrast, SARS-CoV-2-infected CFTR KO cells exhibited fewer lipid droplets scattered in the cytoplasm than their mock-infected counterparts, which were not identifiable as lipolysosomes due to the absence of an external membrane.…”

Section: Discussionmentioning

confidence: 99%

Loss of CFTR Reverses Senescence Hallmarks in SARS-CoV-2 Infected Bronchial Epithelial Cells

Merigo,

Lagni,

Boschi

et al. 2024

IJMS

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SARS-CoV-2 infection has been recently shown to induce cellular senescence in vivo. A senescence-like phenotype has been reported in cystic fibrosis (CF) cellular models. Since the previously published data highlighted a low impact of SARS-CoV-2 on CFTR-defective cells, here we aimed to investigate the senescence hallmarks in SARS-CoV-2 infection in the context of a loss of CFTR expression/function. We infected WT and CFTR KO 16HBE14o-cells with SARS-CoV-2 and analyzed both the p21 and Ki67 expression using immunohistochemistry and viral and p21 gene expression using real-time PCR. Prior to SARS-CoV-2 infection, CFTR KO cells displayed a higher p21 and lower Ki67 expression than WT cells. We detected lipid accumulation in CFTR KO cells, identified as lipolysosomes and residual bodies at the subcellular/ultrastructure level. After SARS-CoV-2 infection, the situation reversed, with low p21 and high Ki67 expression, as well as reduced viral gene expression in CFTR KO cells. Thus, the activation of cellular senescence pathways in CFTR-defective cells was reversed by SARS-CoV-2 infection while they were activated in CFTR WT cells. These data uncover a different response of CF and non-CF bronchial epithelial cell models to SARS-CoV-2 infection and contribute to uncovering the molecular mechanisms behind the reduced clinical impact of COVID-19 in CF patients.

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“…These structures, derived from LDs or other cellular membranes, serve as protective compartments for viral RNA replication. The association with LDs helps shield viral RNA molecules from host immune responses [73].…”

Section: Ld and Viruses In Generalmentioning

confidence: 99%

Lipid Droplets: Formation, Degradation, and Their Role in Cellular Responses to Flavivirus Infections

Hsia,

Liu,

Haynes

et al. 2024

Microorganisms

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Lipid droplets (LDs) are cellular organelles derived from the endoplasmic reticulum (ER), serving as lipid storage sites crucial for maintaining cellular lipid homeostasis. Recent attention has been drawn to their roles in viral replication and their interactions with viruses. However, the precise biological functions of LDs in viral replication and pathogenesis remain incompletely understood. To elucidate the interaction between LDs and viruses, it is imperative to comprehend the biogenesis of LDs and their dynamic interactions with other organelles. In this review, we explore the intricate pathways involved in LD biogenies within the cytoplasm, encompassing the uptake of fatty acid from nutrients facilitated by CD36-mediated membranous protein (FABP/FATP)-FA complexes, and FA synthesis via glycolysis in the cytoplasm and the TCL cycle in mitochondria. While LD biogenesis primarily occurs in the ER, matured LDs are intricately linked to multiple organelles. Viral infections can lead to diverse consequences in terms of LD status within cells post-infection, potentially involving the breakdown of LDs through the activation of lipophagy. However, the exact mechanisms underlying LD destruction or accumulation by viruses remain elusive. The significance of LDs in viral replication renders them effective targets for developing broad-spectrum antivirals. Moreover, considering that reducing neutral lipids in LDs is a strategy for anti-obesity treatment, LD depletion may not pose harm to cells. This presents LDs as promising antiviral targets for developing therapeutics that are minimally or non-toxic to the host.

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Lipid Metabolism Modulation during SARS-CoV-2 Infection: A Spotlight on Extracellular Vesicles and Therapeutic Prospects

Cited by 8 publications

References 159 publications

Consequences of COVID-19 on Adipose Tissue Signatures

Consequences of COVID-19 on Adipose Tissue Signatures

Loss of CFTR Reverses Senescence Hallmarks in SARS-CoV-2 Infected Bronchial Epithelial Cells

Lipid Droplets: Formation, Degradation, and Their Role in Cellular Responses to Flavivirus Infections

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